ABSTRACT
Solitary fibrous tumours are rare mesenchymal tumours which mostly arise from pleura. Such tumours occurring in the mesocolon are exceptionally rare. A 35-year-old man was referred to the general surgery department with a painless and nonpalpable mass in the right quadrant of the abdomen, which was detected incidentally on magnetic resonance imaging. The patient had no symptoms and the physical examination revealed no findings. The patient underwent surgical resection and excisional biopsy results revealed an intra-abdominal solitary fibrous tumour originating from the ascending mesocolon. He was discharged two days after surgery and remained disease-free at the end of the two-month follow-up period.
Subject(s)
Mesocolon , Peritoneal Neoplasms/diagnosis , Solitary Fibrous Tumors/diagnosis , Adult , Humans , Incidental Findings , Magnetic Resonance Imaging , Male , Mesocolon/diagnostic imaging , Mesocolon/pathology , Mesocolon/surgery , Peritoneal Neoplasms/diagnostic imaging , Peritoneal Neoplasms/pathology , Peritoneal Neoplasms/surgery , Solitary Fibrous Tumors/diagnostic imaging , Solitary Fibrous Tumors/pathology , Solitary Fibrous Tumors/surgeryABSTRACT
The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor that mediates many of the biological and toxicological actions of a diverse range of chemicals, including the environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin). Although no endogenous physiological ligand for the AhR has yet been described, numerous studies support the existence of such a ligand(s). Here we have examined the ability of prostaglandins and related chemicals to activate the AhR signaling system. Using two AhR-based bioassay systems we report that relatively high concentrations of several prostaglandins (namely, PGB3, PGD3, PGF3alpha, PGG2, PGH1, and PGH2) can not only stimulate AhR transformation and DNA binding in vitro, but also induce AhR-dependent reporter gene expression in mouse hepatoma cells in culture. PGG2 also induced AhR-dependent reporter gene expression to a level three-to four fold greater than that observed with a maximal inducing dose of TCDD. Sucrose gradient ligand binding analysis revealed that PGG2 could competitively displace [3H]TCDD from the AhR. Overall, our results demonstrate that selected prostaglandins are weak agonists for the AhR and they represent a structurally distinct and novel class of activator of the AhR signal transduction pathway.
